Transcript ACS .CHF. PE - Medical Groupf2

60 year old Female with history of DM2 for 20 years, HTN, HLD
who presented to the ED with 4 hour onset of chest pain which
was described as in the anterior chest without radiation.
VS: T 36.9, HR: 110, BP: 84/56, RR 22, O2 sat. 93% RA.
CHEST PAIN D.Dx ????
Definition: a constellation of symptoms related to obstruction of
coronary arteries with chest pain being the most common
symptom in addition to nausea, vomiting, diaphoresis etc.
Chest pain concerned for ACS is often radiating to the left arm or
angle of the jaw, pressure-like in character, and associated with
nausea and sweating. Chest pain is often categorized into typical
and atypical angina.
Pathophysiology of ACS
• Plaque rupture and subsequent formation of
thrombus – this can be either occlusive or nonocclusive (STEMI, NSTEMI, USA)
• Vasospasm such as that seen in Prinzmetal’s
angina, cocaine use (STEMI, NSTEMI, USA)
• Progression of obstructive coronary
atherosclerotic disease (USA)
• In-stent thrombosis (early post PCI)
• In-stent restenosis (late post PCI
• Poor surgical technique (post CABG)
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Stable: There is a stable pattern of onset, duration and
intensity of sx, pain is triggered by a predictable degree of
exertion or emotion.
Variant Angina (Prinzmetal's)
Cyclical, may occur at rest.
Ventricular arrhythmia, brady arrhythmia and
conduction disturbances occur.
Syncope associated with arrhythmia may occur
Nocturnal Angina only at night. Possible associated
with REM sleep.
Unstable Angina Pre infarction angina
Pain is more intense, lasts longer
 STEMI:
 Q waves , ST elevations, hyper acute T waves; followed by T wave
inversions.
 Clinically significant ST segment elevations:
> than 1 mm (0.1 mV) in at least two anatomical contiguous leads
 or 2 mm (0.2 mV) in two contiguous precordial leads (V2 and V3)
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ST ELEVATION D.DX ????
 NSTEMI:
 ST depressions (0.5 mm at least) or T wave inversions ( 1.0 mm at least)
without Q waves in 2 contiguous leads with prominent R wave or R/S
ratio >1.
 Isolated T wave inversions:
can correlate with increased risk for MI
 may represent Wellen’s syndrome:
 critical LAD stenosis
 >2mm inversions in anterior precordial leads
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 Unstable Angina:
 May present with nonspecific or transient ST segment depressions or
elevations
STEMI Management
 STEMI patients usually go straight to the cath lab from the ED.
Goal: door to balloon 90 minutes.
 Initial management for STEMI:
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Cardiac monitor
Supplemental O2
Nitrates*
Beta blocker
Morphine
Clopidogrel
Aspirin
Good IV access
Call cardiology fellow!
Treatment
Acute Angina Treatment
Goal: Enhance 02 supply to myocardium:
M- Morphine for pain
O- Oxygen 4-6L as ordered
N- NTG sublingual, repeat q5 minutes x3
A- Aspirin to prevent platelet aggregation
THROMBOLYTICS THERAPY
• 66-year-old feman with a history of deep venous thrombosis (DVT)
presented with acute dyspnea , chest pain and palpiation since 42
hours
• Bp 110/80
• RR26
• HR120
• SPO2 84%
• TEMP 37 C
ECG FINDINGS
TYPES
THROMBOEMBOLIC
AIR EMBOLISM
FAT EMBOLISM
RISK FACTORS :
•Hypercoagulable states
•Immobilization
•Surgery and trauma
•Pregnancy
•Oral contraceptives and estrogen replacement
•Malignancy
•Hereditary factors resulting in a hypercoagulable state
•Acute medical illness
•Drug abuse (intravenous [IV] drugs)
•Drug-induced lupus anticoagulant
•Hemolytic anemias
•Heparin-associated thrombocytopenia
•Homocystinemia
•Homocystinuria
•Hyperlipidemias
•Phenothiazines
•Thrombocytosis
•Varicose veins
•Venography
•Venous pacemakers
•Venous stasis
•Warfarin (first few days of therapy)
•Inflammatory bowel disease
P/E :
•Tachypnea (respiratory rate >16/min): 96%
•Rales: 58%
•Accentuated second heart sound: 53%
•Tachycardia (heart rate >100/min): 44%
•Fever (temperature >37.8°C): 43%
•Diaphoresis: 36%
•S 3 or S 4 gallop: 34%
•Clinical signs and symptoms suggesting thrombophlebitis: 32%
•Lower extremity edema: 24%
•Cardiac murmur: 23%
•Cyanosis: 19%
LABORATORY :
•D-dimer testing
•Ischemia-modified albumin level
•White blood cell count
•Arterial blood gases:
•Serum troponin levels
•Brain natriuretic peptide
Table 1. Modified Wells Prediction Rule for Diagnosing Pulmonary Embolism:
Clinical Evaluation Table for Predicting Pretest Probability of Pulmonary Embolism*
Clinical Characteristic
Score
Previous pulmonary embolism or deep vein thrombosis
+ 1.5
Heart rate >100 beats per minute
+ 1.5
Recent surgery or immobilization (within the last 30 d)
+ 1.5
Clinical signs of deep vein thrombosis
+3
Alternative diagnosis less likely than pulmonary
embolism
+3
Hemoptysis
+1
Cancer (treated within the last 6 mo)
+1
Clinical Probability of Pulmonary Embolism
Score
Low
0-1
Intermediate
2-6
High
≥6
*Reprinted from Am J Med, Vol. 113, Chagnon I, Bounameaux H, Aujesky D, et al, Comparison of two clinical
prediction rules and implicit assessment among patients with suspected pulmonary embolism, pp 269-75,
Copyright 2002.
Imaging studies
•Computed tomography angiography (CTA): Multidetector-row CTA (MDCTA) is the criterion standard for diagnosing pulmonary
embolism
•Pulmonary angiography: Criterion standard for diagnosing pulmonary embolism when MDCTA is not available
•Chest radiography: Abnormal in most cases of pulmonary embolism, but nonspecific
•V/Q scanning: When CT scanning is not available or is contraindicated
•ECG: Most common abnormalities are tachycardia and nonspecific ST-T wave abnormalities
•MRI: Using standard or gated spin-echo techniques, pulmonary emboli demonstrate increased signal intensity within the
pulmonary artery
•Echocardiography: Transesophageal echocardiography may identify central pulmonary embolism
•Venography: Criterion standard for diagnosing DVT
•Duplex ultrasonography: Noninvasive diagnosis of pulmonary embolism by demonstrating the presence of a DVT at any site
X RAY FINDINGS :
Common radiographic abnormalities include atelectasis, pleural effusion, parenchymal opacities, and elevation of a
hemidiaphragm. The classic radiographic findings of pulmonary infarction include a wedge-shaped, pleura-based triangular
opacity with an apex pointing toward the hilus (Hampton hump) or decreased vascularity (Westermark sign). These findings
are suggestive of pulmonary embolism but are infrequently observed.
A prominent central pulmonary artery (knuckle sign), cardiomegaly (especially on the right side of the heart), and pulmonary
edema are other findings
Management
Anticoagulation medications include the following:
•Unfractionated heparin
•Low-molecular-weight heparin
•Fondaparinux
•Warfarin
Thrombolytic agents used in managing pulmonary embolism include the following:
•Alteplase
•Reteplase
•Urokinase
•Streptokinase
Surgical options
Surgical management options include the following:
•Catheter embolectomy and fragmentation or surgical embolectomy
•Placement of vena cava filters
Potential indications for thrombolytic therapy in venous thromboembolism
Presence of hypotension related to PE*
Presence of severe hypoxemia
Substantial perfusion defect
Right ventricular dysfunction associated with PE
Extensive deep vein thrombosis
• 67 YS OLD FEMALE , DM ,HTN ,CHRONIC RENAL IMPAIRMENT
• PRESENTED WITH SEVER SOB , SHALLOW BREATHING FOR 1 HOUR AT
HOME
• BP 220/130
• HR130
• RR30
• SPO2 70% RA
• TEMP 38C
Classifications- (how to describe)
• Systolic versus diastolic
• Systolic- loss of contractility get dec. CO
• Diastolic- decreased filling or preload
• Left-sided versus right –sided
• Left- lungs
• Right-peripheral
• High output- hypermetabolic state
• Acute versus chronic
• Acute- MI
• Chronic-cardiomyopathy
Heart Failure
Etiology and Pathophysiology
• Primary risk factors
• Coronary artery disease (CAD)
• Advancing age
• Contributing risk factors
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Hypertension
Diabetes
Tobacco use
Obesity
High serum cholesterol
African American descent
Valvular heart disease
Hypervolemia
Symptoms
DIAGNOSIS :
The American College of Cardiology/American Heart Association (ACC/AHA),[3] Heart Failure Society of America (HFSAand
European Society of Cardiology (ESC) recommend the following basic laboratory tests and studies in the initial evaluation of
patients with suspected heart failure:
•Complete blood count (CBC), which may indicate anemia or infection as potential causes of heart failure
•Urinalysis (UA), which may reveal proteinuria, which is associated with cardiovascular disease
•Serum electrolyte levels, which may be abnormal owing to causes such as fluid retention or renal dysfunction
•Blood urea nitrogen (BUN) and creatinine levels, which may indicate decreased renal blood flow
•Fasting blood glucose levels, because elevated levels indicate a significantly increased risk for heart failure (diabetic and
nondiabetic patients)
•Liver function tests (LFTs), which may show elevated liver enzyme levels and indicate liver dysfunction due to heart failure
•B-type natriuretic peptide (BNP) and N-terminal pro-B-type (NT-proBNP) natriuretic peptide levels, which are increased in
heart failure; these measurements are closely correlated with the NYHA heart failure classification
•Electrocardiogram (ECG) (12-lead), which may reveal arrhythmias, ischemia/infarction, and coronary artery disease as
possible causes of heart failure
IMAGING STUDY :
• CXR
• ECHO
TREATMENT :
• A 35-year-old man presents to the emergency department with pleuritic
chest pain that began about 7 hours ago. He states that the pain is sharp,
radiates to his left shoulder, and is alleviated by leaning forward. He
reports having flu-like symptoms for the past week. He is worried that he is
having a heart attack because he has a
• “lousy” family history. Which of the following would make a acute
myocardial infarction (MI) as a diagnosis in this patient most unlikely?
• (A) Absence of Q waves on the electrocardiogram (ECG)
• (B) Lack of response to a trail of nitroglycerin (NTG)
• (C) The patient’s young age
• (D) Radiation of the pain to the left shoulder
• (E) Positive family history
• Nitroglycerin (NTG) therapy is contraindicated for which of the
following?
• (A) Unstable angina
• (B) Anterior wall myocardial infarction (MI)
• (C) Inferior wall MI
• (D) Right ventricular MI
• (E) Lateral wall MI
• Which of the following electrocardiogram patterns is most consistent
with occlusion of the right coronary artery?
• (a) ST-segment elevation in V1, V2 and V3.
• (b) R waves in V1 and V2 > 0.04 s and R/S ratio ≥ 1.
• (c) ST-segment elevation is I and aVL.
• (d) ST-segment elevation in II, III, and aVF
• An 85-year-old female presents with acute onset of dyspnea,
inspiratory rales, and holosystolic murmur. Her electrocardiogram
reveals Q waves in II, III and aVF. Approximately five days earlier, she
relates, she had a "severe bout of heartburn." Cardiac enzymes are
significant for a normal CK-MB but elevated troponin. What is the
most likely cause of this patient's symptoms?
• (a) Left ventricular free wall rupture.
• (b) Pulmonary embolism
• . (c) Dressler syndrome.
• (d) Papillary muscle rupture
• Which of the following therapeutic agents has been shown to
unequivocally decrease mortality in the setting of acute myocardial
infraction?
• (a) Aspirin
• (b) Calcium channel antagonisits.
• (c) Magnesium.
• (d) Glycoprotein IIb/IIIa inhibito
• A 50-year-old male presents with an acute inferior wall myocardial
infraction, following the administration of aspirin and nitroglycerin, he
suddenly becomes confused and diaphoretic with a blood pressure of
70/30 mmHg. Physical examination reveals jugular venous distention, clear
lung fields, and no evidence of murmur. What combination of therapeutic
agents is most likely to immediately stabilize this patient?
• (a) Heparin and glycoprotein IIb/IIIa inhibitors.
• (b) Angiotensin converting enzyme inhibitor and clopidogrel.
• (c) Streptokinase and magnesium.
• (d) Normal saline bolus and dobutamine
Which of the following is NOT part of Virchow's triad of risk
factors for venous thromboembolism?
(a) Venous stasis.
(b) Malignancy.
(c) Vessel wall injury.
(d) Hypercoagulable stat